The GPIa C807T dimorphism associated with platelet collagen receptor density is not a risk factor for myocardial infarction

Croft, S. A.; Hampton, K. K.; Sorrell, Julian; Steeds, Richard P.; Channer, Kevin S.; Samani, Nilesh J.; Daly, Mary E.

doi:10.1046/j.1365-2141.1999.01597.x

Cited by 64 publications

(42 citation statements)

References 20 publications

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“…The highdensity GPIa 807T/873A allele frequency was not reported to be a risk factor for venous thrombosis among this patient cohort [6]. The high-density allele 807T/873A has been found to be associated with increased risk of myocardial infarction in two independent studies [3,7], whereas was reported by another group [8].…”

Section: Introductionmentioning

confidence: 58%

Platelet glycoprotein Ia 807C/T (Phe224) and 873G/A (Thr246) dimorphisms in Turkey

Komurcu

Erginel-Unaltuna

2001

American J Hematol

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At sites of vascular injury, the platelet collagen receptor Glycoprotein Ia/IIa (GPIa/IIa) acts as an important mediator of platelet adhesion to ®brillar collagens. Two silent polymorphisms (807C/T and 873G/A) within the glycoprotein Ia gene have been implicated in increased risk of developing thrombosis and myocardial infarction in affected individuals. To provide basis for future studies, we examined the frequency of these GPIa polymorphisms for people in Turkey. We analyzed 118 unrelated individuals for their genotypes of the GPIa gene using a multiplexed allele speci®c-PCR based method. The allelic frequencies were found to be 34% for 807T/873A and 66% for 807C/873G; the genotypic frequencies were 13% for 807TT/873AA, 44% for 807CT/873GA, and 43% for 807CC/873GG. Am.

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Section: Introductionmentioning

confidence: 58%

Platelet glycoprotein Ia 807C/T (Phe224) and 873G/A (Thr246) dimorphisms in Turkey

Komurcu

Erginel-Unaltuna

2001

American J Hematol

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“…41 Several studies have shown that polymorphisms of GpIa/IIa may be associated with large vessel arterial disease, and our identification that they also play a role in RVO suggests a common genetic link and may explain the higher risk of MI in RVO patients. [19][20][21][22][23] In conclusion, our study suggests a major, possibly pivotal role for polymorphisms of the platelet glycoprotein receptor GpIa/IIa in the pathogenesis of RVO. Although larger studies allowing multivariate analysis will be required to confirm our findings, these data present for the first time a potential genetic marker that could have major implications for the aetiology and management of microvascular disease, in this case RVO.…”

Section: Discussionmentioning

confidence: 85%

“…Given the importance of GpIa/IIa in primary haemostasis, several studies have assessed the roles of these polymorphisms in both large vessel venous and arterial thrombosis including myocardial infarction (MI), stroke, deep venous thrombosis, and pulmonary embolism. [18][19][20][21][22][23] Although results are conflicting, it appears that GpIa/IIa polymorphisms may play a role in large vessel arterial but not venous thrombosis and its role in microvascular disease is unknown. We know however that GpIa/IIa polymorphisms play a major role in retinal vessel disease.…”

Section: Introductionmentioning

confidence: 99%

The platelet glycoprotein Ia/IIa gene polymorphism C807T/G873A: a novel risk factor for retinal vein occlusion

Dodson

Haynes

Starczynski

et al. 2003

Eye

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Retinal vein occlusion (RVO) is associated with hyperhomocysteinaemia and the antiphospholipid syndromeFdisorders known to contribute to both arterial and venous thrombosis. In both of these conditions and RVO, platelet activation occurs. Aspirin, not warfarin, is the most effective antithrombotic agent in RVO and, taken together, these observations suggest an important role for platelets in this common ocular thrombotic condition. Platelet glycoprotein Ia/IIa (GpIa/IIa) is an adhesion molecule mediating platelet-collagen interactions and is key to the initiation of thrombosis. Recently, the cellular density of this molecule was shown to be determined by two silent, linked polymorphisms (C807T/ G873A) within the GpIa/IIa gene. There is evidence that some of the resulting genotypes are associated with thrombo-embolic disease. This study therefore aimed to establish the prevalence of the GpIa/IIa polymorphisms and the three commonest hereditary thrombophilic disorders (prothrombin gene G20210A (PT) mutation, Factor V Leiden (FVL), and the thermolabile methylene tetrahydrofolate reductase C677T (MTHFR) mutation) in patients with RVO and normal controls. The GpIa/IIa polymorphisms and thrombophilic abnormalities were all identified using the polymerase chain reaction. Our results show that the frequency of the GpIa/IIa polymorphisms was similar in our normal control population to previously published series. Patients with RVO, however, had only a 10% (4/40) frequency of the lowest risk subtype (CC/GG) compared to 37.5% (15/40) in the control groupFP 0.0039.The incidence of the PT, FVL, and MTHFR thrombophilic mutations was not different between the two groups, but interestingly none of the 7/40 RVO cases with a PT, FVL, or MTHFR mutation had the low-risk GpIa/IIa genotype while all but one of the controls didFPo0.05. Thus, 17.5% of RVO patients harboured more than one prothrombotic abnormality. The principal difference between the RVO and control group was the very high incidence of the intermediate-risk GpIa/IIa subtype (CT/GA)F82.5 vs 50%, Po0.05. These results suggest a major role for GpIa/IIa polymorphisms in the pathogenesis of RVO.

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“…1,2 We recently showed that the 807T allele of the GP Ia gene that is associated with increased GP Ia/IIa expression and platelet adhesiveness to collagen did not confer an increased risk of myocardial infarction (MI) and proposed that polymorphic variation at the GP VI locus might contribute to an increased risk of bleeding or thrombosis under certain circumstances. 3 In the present study, analysis of the GP VI gene sequence in a panel of healthy subjects resulted in identification of 10 GP VI gene dimorphisms. The effect of one of these dimorphisms on risk of MI was then assessed.…”

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confidence: 71%

“…Further details of recruitment were described previously. 3 The study received local ethics committee approval in both centers.…”

Section: Subjectsmentioning

confidence: 99%

Novel Platelet Membrane Glycoprotein VI Dimorphism Is a Risk Factor for Myocardial Infarction

et al. 2001

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Background-Glycoprotein (GP) VI plays a crucial role in platelet activation and aggregation. We investigated whether polymorphic variation at the GP VI locus confers an increased risk of myocardial infarction (MI). Methods and Results-Coding and 5Ј and 3Ј non-coding regions of the GP VI gene were analyzed by polymerase chain reaction and conformation sensitive gel electrophoresis in 21 healthy subjects. Ten dimorphisms, 5 of which predicted amino acid substitutions (T13254C, A19871G, A21908G, A22630T, C22644A), were identified. Two core haplotypes involving 7 dimorphisms (C10781A and G10873A and all those predicting amino acid substitutions) were apparent.

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The GPIa C807T dimorphism associated with platelet collagen receptor density is not a risk factor for myocardial infarction

Cited by 64 publications

References 20 publications

Platelet glycoprotein Ia 807C/T (Phe224) and 873G/A (Thr246) dimorphisms in Turkey

Platelet glycoprotein Ia 807C/T (Phe224) and 873G/A (Thr246) dimorphisms in Turkey

The platelet glycoprotein Ia/IIa gene polymorphism C807T/G873A: a novel risk factor for retinal vein occlusion

Novel Platelet Membrane Glycoprotein VI Dimorphism Is a Risk Factor for Myocardial Infarction

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